The inner surface and capsule of joints is lined by a delicate vascular connective tissue known as the synovial membrane. In rheumatoid arthritis (RA) and related conditions, the synovial membrane becomes massively hypertrophic and inflamed. The objectives of this study are to characterize these tissues in terms of the molecular mediators involved in generating the pathologic change. We have been particularly interested in factors mediating (angiogenesis). We have shown that interleukin-1 and prostaglandin E2 are powerful stimulators of vascular endothelial growth factor (VEGF), which is highly expressed in rheumatoid joints (Ben-Av et al., FEBS Letters 372, 83, 1995). Since both interleukin-1 and prostaglandin E2 are suppressed by corticosteroids, the data provide new insights into the interactions of corticosteroids and its potential role in regulating disease expression in RA.